Singlet oxygen, O2-, has been identified as a potential atmospheric oxidant. Although its steady state concentration in the atmosphere is low, O2- is sufficiently long-lived to react with pollutants such as olefins and polycyclic hydrocarbons to form toxic or potentially mutagenic compounds. The relatively long lifetime of O2- suggests that it may reach the lung by inhalation. Current research indicates that O2- may be formed in the lung, e.g., by the reaction of ozone with biological substrates. In the lung, one initiating event can lead to the oxidation of many biomolecules. O2- can produce subtle chemical changes in the tracheal bronchial epithelium, alveolar surfactant, and macrophages that can predispose to various pathological conditions. O2- attacks the unsaturated fatty acid moieties of lipids to form hydroperoxides via the "ene" reaction; lipid epoxides and malonylaldehyde may form by secondary reactions. The hydroperoxides are known to cause lung inflammation, edema, and hemorrhaging. Malonylaldehyde and lipid epoxides can act as alkylating agents and ultimately lead to cancer. The involvement of O2- in the chemical events that lead to these biological effects needs to be uniquivocally demonstrated. The research will (1) continue to investigate the laboratory generation of O2- by heterogeneous photosensitization and additional O2-forming environmental reactions, (2) study the reaction of O2- with model membrane systems, i.e., liposomes of synthetic lipids, to determine the chemical mechanisms by which O2- initiates biological damage, and (3) complete in vitro exposure of hamster tracheal epithelium. The overall goal of the research is to determine if there is a link between atmospherically generated O2- and some of the adverse health effects attributed to air pollution.